Alzheimer’s disease: from early pathogenesis to novel therapeutic approaches
Abstract
The mainstay behind Alzheimer's disease (AD) remains unknown due to the elusive pathophysiology of the disease. Beta-amyloid and phosphorylated Tau is still widely incorporated in various research studies while studying AD. However, they are not sufficient. Therefore, many scientists and researchers have dug into AD studies to deliver many innovations in this field. Many novel biomarkers, such as phosphoglycerate-dehydrogenase, clusterin, microRNA, and a new peptide ratio (Aβ37/Aβ42) in cerebral-spinal fluid, plasma glial-fibrillary-acidic-protein, and lipid peroxidation biomarkers, are mushrooming. They are helping scientists find breakthroughs and substantiating their research on the early detection of AD. Neurovascular unit dysfunction in AD is a significant discovery that can help us understand the relationship between neuronal activity and cerebral blood flow. These new biomarkers are promising and can take these AD studies to another level. There have also been big steps forward in diagnosing and finding AD. One example is self-administered-gerocognitive-examination, which is less expensive and better at finding AD early on than mini-mental-state-examination. Quantum brain sensors and electrochemical biosensors are innovations in the detection field that must be explored and incorporated into the studies. Finally, novel innovations in AD studies like nanotheranostics are the future of AD treatment, which can not only diagnose and detect AD but also offer treatment. Non-pharmacological strategies to treat AD have also yielded interesting results. Our literature review spans from 1957 to 2022, capturing research and trends in the field over six decades. This review article is an update not only on the recent advances in the search for credible biomarkers but also on the newer detection techniques and therapeutic approaches targeting AD.
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Tau hyperphosphorylation disrupts microtubule stability, promotes intraneuronal aggregates, synaptic dysfunction, and neuronal loss.
“Tau hyperphosphorylation disrupts microtubule stability, promotes intraneuronal aggregates, synaptic dysfunction, and neuronal loss [5,6].”
From Theranostic Nanoplatforms for Alzheimer's Disease: A Critical Analysis of Conceptual Contradictions (2026) · cites this paper as [6]
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Influential
- Authors
- Prajapati, S. K., Pathak, A., & Samaiya, P. K.
- Affiliations
- University of South Florida (US)
- Shri Govindram Seksaria Institute of Technology and Science (IN)
- Corresponding author
- Samaiya, Puneet K.
- Venue
- Metabolic Brain Disease
- Published
- 2024-07-24
- Volume
- 39
- Issue
- 6
- Pages
- 1231-1254
- ISSN
- 0885-7490 (ISSN-L)
- 1573-7365
- OpenAlex
- W4400958101
- Cited by
- 21
- References
- 232
- Citations by year
- 2026: 11 · 2025: 10
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Metabolic Brain Disease (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, Alzheimer's disease pathogenesis, Alzheimer's disease biomarkers, amyloid-beta, phosphorylated tau, PHGDH, clusterin, microRNA, glial fibrillary acidic protein, lipid peroxidation, cerebral blood flow, early detection, electrochemical biosensor, nanotheranostics, non-pharmacological treatment, treatment options
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Biomarkers, Amyloid beta-Peptides, Early Diagnosis
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